Ahmed Abdel Salam
El Sheikh Zayed Al Nahian Hospital, Egypt
Title: Interleukin-1 and interleukin-18 as mediators of inflammation and the aging process
Biography
Biography: Ahmed Abdel Salam
Abstract
Oxidative stress and low-grade inflammation are hallmarks of aging process as mitochondrial dysfunction and oxidative stress induce multi-protein inflammatory complexes called inflammasomes. Nod like receptor protein 3 (NLRP3) major immune sensors for cellular stress signals, e.g. reactive oxygen species cathepsin B NLRP3 activation triggers caspase1 mediated maturation of IL-1b and IL-18. IL-1b and IL-18 are of the same family closely related similar 3-dimensional structure their precursors are inactive until cleaved by intracellular cysteine protease caspase. NLRP3 gene control activity of caspase1 as NLRP3 gene participate in conversion of procaspase-1 to active caspase1 so mutation in NLRP3 gene will affect IL-1b and IL-18 secretion during aging. Autophagic clearance of mitochondria declines and dysfunctional mitochondria provoke oxidative stress disturb cellular redox balance. During aging increased NF-Kb potentiate expression of NLRP3 and cytokines inflammasomes play role in proinflammatory phenotype during aging process and IL-1b and IL-18 participate in fundamental inflammatory process that increased during aging process